Figure 5.

Tumor formation by PRL3 mutants. A, lysates of B16 mouse melanoma cells stably expressing the indicated constructs were subjected to immunoblotting analyses with Myc antibody to check expression levels of each PRL3 mutant. Staining for β-tubulin was used as a loading control. B, B16 cells were injected into mice via their tail veins. 3 weeks later, they were sacrificed, the lungs were removed, and tumor nodules were counted. C, number of tumor nodules per mouse. Stable expression of PRL3 WT and C104D mutant significantly augmented the number of tumor nodules. The catalytically active R138E, which is defective in CNNM binding, showed the same number of nodules as the GFP control. The bar graph shows the average ± S.D. (n = 6 for GFP, Myc-PRL3-C104E, and Myc-PRL3-R138E; n = 12 for Myc-PRL3-WT and Myc-PRL3-C104D).